Dr. Stephen Chung received his medical degree at Washington University School of Medicine in 2006, followed by an internship and residency in internal medicine at Massachusetts General Hospital and a medical oncology fellowship at Memorial Sloan Kettering Cancer Center (MSKCC). He subsequently joined the faculty of the Leukemia Service at MSKCC while conducting his postdoctoral studies in the labs of Christopher Park and Ross Levine.
In his postdoctoral studies he applied his training in hematopoiesis and stem cell biology to contribute towards our understanding of disease initiating stem cells in several hematologic malignancies including acute myeloid leukemia (AML), the myelodysplastic syndromes (MDS), and hairy cell leukemia (HCL).
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Dr. Stephen Chung received his medical degree at Washington University School of Medicine in 2006, followed by an internship and residency in internal medicine at Massachusetts General Hospital and a medical oncology fellowship at Memorial Sloan Kettering Cancer Center (MSKCC). He subsequently joined the faculty of the Leukemia Service at MSKCC while conducting his postdoctoral studies in the labs of Christopher Park and Ross Levine.
In his postdoctoral studies, he applied his training in hematopoiesis and stem cell biology to contribute towards our understanding of disease initiating stem cells in several hematologic malignancies including acute myeloid leukemia (AML), the myelodysplastic syndromes (MDS), and hairy cell leukemia (HCL).
A common thread to his work has been the use of primary patient specimens to gain important insights into disease biology. Although HCL had long been considered to be a mature B-cell malignancy, he unexpectedly identified disease associated BRAF V600E mutations in hematopoietic stem cells from patients with hairy cell leukemia, going on to demonstrate using mouse models that BRAF mutations must arise at the earliest stages of hematopoiesis to give rise to “mature” disease cells. These findings exemplify a new paradigm for understanding mature lymphoid malignancies such as chronic lymphocytic leukemia and non-Hodgkins lymphoma, and they have already informed the design of ongoing clinical trials.
In other work, he assessed a large number of primary AML and MDS specimens to identify CD99 as one of the most frequently upregulated cell surface markers present on malignant stem cells in these diseases. His characterization of CD99 demonstrated that it can be used to prospectively isolate and enrich for functional human leukemic stem cells (LSCs), providing a new tool that may allow for selective depletion of LSCs from patient bone marrows, as well as improved studies of LSCs in the lab. He has identified and generated monoclonal antibodies directed towards CD99 that are directly toxic to AML and MDS stem cells, with these studies forming the basis for ongoing work developing CD99-directed therapeutics.
Most recently, he has been performing work studying single cell transcriptomes of MDS stem cells to identify mechanisms of resistance to therapy. By examining MDS HSCs taken from patients over the course of HMA therapy, he has identified gene signatures predictive of resistance to therapy, as well as unique subpopulations of MDS HSCs that may underlie disease relapse and which would not have been detected using conventional bulk sequencing methods.
Dr. Chung has recently identified a novel function for CD99 in the regulation of translation, and his lab at UT Southwestern will study the mechanisms by which this function regulates self-renewal in normal and malignant stem cells in the hematopoietic system. Given that stem cells are particularly sensitive to perturbations in protein synthesis, the lab is also investigating modalities by which translation can be disrupted selectively in disease stem cells.
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